The resilience of teeth depends on a complex interplay between mineral (termed hydroxyapatite) and organic components (proteins, cells and tissues). Under normal conditions the hydroxyapatite in enamel and dentine is organised into an extraordinarily dense structure that confers the hardness and toughness required for maintenance of the tooth's integrity. Loss of mineral-density in enamel and dentine results in abnormally porous hydroxyapatite, which compromises the tooth's physical resilience and can lead to structural failure. Porous hydroxyapatite is caused by several prevalent conditions, including dental caries and developmental dental defects (DDD).
Dental caries (tooth decay) is a disease caused by bacteria that secrete acid. The acid produced by cariogenic bacteria can dissolve hydroxyapatite in a process termed demineralisation. The initial process of demineralisation (termed incipient caries) leads to discrete regions of porous hydroxyapatite termed white spot lesions. Over time, a white-spot lesion may progress to a cavity (i.e. loss of tooth material) or it may stall (termed inactive caries) and re-form a dense hydroxyapatite shell in a process called remineralisation. Before a cavity forms, the process is reversible (i.e. remineralisation), but once enamel is lost it cannot be regenerated.
Caries is diagnosed by a combination of visual inspection, physical challenge (e.g. scratching with dental probe), and X-ray radiography (to detect caries between teeth or beneath the gum line). Worryingly, these diagnostic approaches miss approximately half of early caries, and up to 13% of teeth diagnosed as carious with these methods are in fact caries-free. Recent attempts at improving diagnosis include use of equipment that measures electrical impedance, quantitative light-induced fluorescence (QLF) and infrared laser fluorescence (DIAGNOdent®), but none have found widespread use because of the cost and size of apparatus, and problems with inter-individual variation. Another approach has been the use of dyes to detect dental caries in dentine. However, these dyes are not selective for porous hydroxyapatite: they bind to proteins (presumed to be associated with infecting bacteria in dentine) or they occupy interstitial space, which reduces specificity and sensitivity. Moreover, these dyes cause the oral cavity to become discoloured, bind to healthy teeth, or require visualisation with an irradiator.
There are two main treatments for caries, the selection of which is dictated by the extent of disease. White spot lesions may be treated with remineralisation approaches (e.g. fluoride therapy or amorphous calcium phosphate stabilised with bioactive molecules). Cavities require conventional restorative dentistry (i.e. fillings).
DDD are another common cause of porous hydroxyapatite. They are disturbingly prevalent and costly, potentially afflicting over 50% of the population with multiple burdens including dental pain, disfigurement and increased caries risk. The two most prevalent DDD are dental fluorosis (characterised by diffuse opacities) and Molar/Incisor Hypomineralisation (MIH; characterised by demarcated opacities); both are caused by environmental agents (i.e. acquired defects). Another serious but rare DDD that can result in porous hydroxyapatite is the genetic disease amelogenesis imperfecta.
MIH typically affects 10-20% of children and is a major risk factor for caries, a risk factor for orthodontics, and is costly to society. MIH is thought to result from a multifactorial systemic disturbance of the enamel-forming cells. However, other than being dissociated from fluoride and linked to illness during infancy, the cause of MIH remains a mystery.
There are currently no products available that are designed to diagnose and repair MIH or other DDD. Differential diagnosis of caries and various DDD can be difficult and is largely dependent upon the experience and skill of individual dental health professionals. Current procedures and/or products developed for remineralisation of caries do not work well on MIH. Restorative treatment is frequently compromised because MIH enamel is soft, porous and poorly delineated from normal tooth tissue.
Accordingly, a need exists for new tools to diagnose, delineate and repair porous dental hydroxyapatite caused by caries and DDD. Here we address this need by detailing new technologies based on our recent discoveries of pathogenic mechanisms in conditions involving porous hydroxyapatite.